Hypothalamic hypernatremia due to volume-dependent ADH release, and its treatment with carbamazepine and clofibrate.

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  • KIMURA TOKIHISA
    The Second Department of Internal Medicine, Tohoku University School of Medicine
  • MATSUI KUNIAKI
    The Second Department of Internal Medicine, Tohoku University School of Medicine
  • OTA KOZO
    The Second Department of Internal Medicine, Tohoku University School of Medicine
  • YOSHINAGA KAORU
    The Second Department of Internal Medicine, Tohoku University School of Medicine

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  • Hypothalamic Hypernatremia Due to Volum

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A 23-year-old man, diagnosed as having a pituitary adenoma at the age of 17 and received an operation 1 month ago showed a fluctuating hypernatremia and hypodipsia. The water deprivation, water load and hypertonic saline infusion tests were carried out. After a 14-hr water deprivation test, plasma osmolality was 310 mOsm/kg, plasma ADH was 1.5 μU/ml, and urine osmolality was 591 mOsm/kg. On the water load test subsequently performed, the plasma osmolality decreased to 297 mOsm/kg, but the urine was still hypertonic. Infusion of 2.5% saline solution elicited paradoxically a marked diuresis and dilution of urine depsite the elevation of plasma osmolality. On the treatment with carbamazepine and clofibrate, the urinary osmolality increased, the hypernatremia was normalized, and a marked natriuresis was elicited with a gain in body weight. These results suggested that the secretion of ADH is regulated by changes in blood volume rather than by the plasma osmolality in this patient. The hypernatremia may be explained as a disturbance or lack of osmoreceptor function for ADH release and the loss of thirst sensation, though the volume receptor still remains functioning for ADH secretion. Depletion of the extracellular fluid volume may be another contributing factor to the elevation of serum sodium level by enhancing the reabsorption of sodium from renal tubules.

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